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ENDOCANNABINOID ANALOGS REDUCE HUMAN RETINAL VASCULAR ENDOTHELIAL CELL PROLIFERATION
Author(s) -
Samudre Sandeep S,
Nicholls Martina,
Williams Patricia B,
Lattanzio Frank A
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.lb404
Subject(s) - ranibizumab , retinal , bevacizumab , cell growth , macular degeneration , angiogenesis , vascular endothelial growth factor , medicine , pharmacology , in vivo , retina , intravitreal administration , cancer research , chemistry , ophthalmology , vegf receptors , biology , neuroscience , chemotherapy , biochemistry , microbiology and biotechnology
Age‐related macular degeneration (AMD) is a leading cause of blindness worldwide, with current treatment regimen based on intravitreal injections of VEGF inhibitors, which are designed to slow the rampant growth of blood vessels that underlies the pathology of this disease. Endocannabinoids represent a new approach to AMD treatment as they have the potential to reduce unwanted blood vessel growth. We hypothesize that novel endocannabinoid analog, O‐1812, will reduce proliferation in human retinal vascular endothelial (hRVE) cells. To test vascular cell growth inhibition, 25nM O‐1812, anti‐VEGFs, bevacizumab or ranibizumab, were applied to hRVE cells during the log growth phase over 24 hrs, 10nM VEGF. Ranibizumab (10 μg/ml) or bevacizumab (2500 μg/ml) reduced cell growth in the presence of VEGF. O‐1812 half maximally inhibited cell growth VEGF. In hRVE cells, O‐1812 reduced cell proliferation in the presence or absence of VEGF. Cannabinoids have the potential to reduce angiogenesis related to AMD in vivo. This study has been supported in part by the Richmond Eye and Ear Foundation, Richmond VA.